Cannabinoids and cell fate.Conclusion:
Regarding the central nervous
system, most of the experimental evidence indicates that cannabinoids may
protect neurons from toxic
insults such as glutamaergic overstimulation, ischemia and oxidative
Conclusion: Most of the experimental
evidence indicates that cannabinoids may protect normal neurons from toxic
Conclusion: The psychotropic cannabinoid
receptor agonist Δ9tetrahydrocannabinol (THC) and cannabidiol,
(a non-psychoactive constituent of marijuana), both reduced NMDA, AMPA and
kainate receptor mediated neurotoxicities.
Conclusion: Excitotoxic neuronal death
underlies many neurodegenerative disorders. This study demonstrates the
importance of agonist efficacy and the duration of treatment on the
neuroprotective effects of cannabinoids.
Conclusion: In glaucoma, the increased
release of glutamate is the major cause of retinal ganglion cell death. In
conclusion, our results indicate that lipid peroxidation and ONOO- formation
play an important role in NMDA-induced retinal neurotoxicity and cell loss in
the retina, and that THC and CBD, by reducing the formation of these compounds,
are effective neuroprotectants.
Memantine and Δ9
-tetrahydrocannabinol alone were without effect, however, co-administration of
the drugs significantly decreased number of haloperidol-induced jaw movements.
The antitremor activity of the combination was antagonized (i) by injections of
L-glutamate into the dorsal striatum, entopeduncular nucleus, substantia nigra
pars reticulata, globus pallidus, supratrigeminal and trigeminal motor nuclei
but not into the subthalamic and cuneiform nuclei; (ii) by injections of CGS
21680 into the ventrolateral striatum; (iii) by injections of bicuculline into
the rostral part of the parvicellular reticular nucleus. The presented results
identify brain areas influencing parkinsonian-like tremor in rats; these data
can help advance the development of novel treatments for repetitive involuntary
Conclusion: Marijuana users were high
functioning, demonstrating comparable IQs to controls and relatively better
processing speed. Marijuana users demonstrated relative cognitive
impairments in verbal memory, spatial working memory,
spatial planning, and motivated decision making but comorbid use of alcohol,
which was heavier in marijuana users, was unexpectedly found to be associated
with better performance in some of these areas.
Conclusion: At the population level, it does
not appear that current illicit drug use is associated with impaired cognitive
functioning in early middle age.
Smoking marijuana resulted
in intoxication, as assessed by a behavioral rating scale, but did not
significantly alter mean behavioral performance on the attention task. There
was no significant rCBF change in the nucleus accumbens or other reward-related
brain regions, nor in basal ganglia or
hippocampus, which have a
high density of cannabinoid receptors.
Conclusion: The researchers conclude that
heavy marijuana use produces no irreversible mental deficits.
Conclusion: We conclude that
marijuana does not have a long-term
negative impact on global intelligence.
Conclusion: Compared with controls,
marijuana users had significantly less bilateral orbitofrontal gyri volume,
higher functional connectivity in the orbitofrontal cortex (OFC) network, and
higher structural connectivity in tracts that innervate the OFC (forceps minor)
as measured by fractional anisotropy (FA)
Conclusion: We found that the brain-injured
animals treated with the agonist showed a marked recovery.
Conclusion: Cannabinoids inhibit cortical
neuron differentiation and promote glial differentiation. On the other hand,
experiments with differentiated neurons have shown that cannabinoids also
regulate neuritogenesis, axonal growth and synaptogenesis.
Conclusion: When 2-AG was administered
together with additional inactive 2-acyl-glycerols that are normally present in
the brain, functional recovery was significantly enhanced.
Conclusion: An ultralow dose of THC that
lacks any psychotrophic activity protects the brain from
neuroinflammation-induced cognitive damage and might be used as an effective
drug for the treatment of neuroinflammatory conditions, including
Conclusion: Our results suggest that CBC
raises the viability of NSPCs while inhibiting their differentiation into
astroglia, possibly through up-regulation of ATP and adenosine signalling.
Conclusion: The team found that rats treated
with HU-210 on a regular basis showed neurogenesis the growth of new
brain cells in the hippocampus. This region
of the brain is associated with learning and memory, as well as anxiety and
depression. The effect is the opposite of most legal and illicit drugs such as
alcohol, nicotine, Heroin, and
Conclusion: The THC(+) group was compared
with the THC(-) group with respect to injury mechanism, severity, disposition,
and mortality. A positive THC screen is associated with decreased mortality in
adult patients sustaining TBI.
Conclusion: Our findings demonstrate that
CBD exerts robust neuroprotective effects in vivo in HI piglets, modulating
excitotoxicity, oxidative stress and inflammation, and that both CB2 and 5HT1A
receptors are implicated in these effects.
Conclusion: These results provide evidence
that the cannabinoid system can serve to protect the brain against
Conclusion: Cannabidiol (CBD), the main
non-psychotomimetic component of the plant Cannabis sativa, exerts
therapeutically promising effects on human mental health such as inhibition of
psychosis, anxiety and depression. However, the
mechanistic bases of CBD action are unclear. Here we investigate the potential
involvement of hippocampal neurogenesis in the anxiolytic effect of CBD
Conclusion: This study provides the first
demonstration of CBD as an in vivo neuroprotectant and shows the efficacy of
lipophilic antioxidants in preventing binge
ethanol induced brain
Conclusion: The endocannabinoid system is
expressed in the intact spinal cord, and it is dramatically upregulated after
Conclusion: Considering that cannabidiol
presents an extremely safe profile and is currently being used clinically,
these results suggest that this compound could be useful in the treatment of
intervertebral disc degeneration.
Conclusion: The findings showed that the
compounds could reduce the size of stroke and improve neurological
Conclusion: Phytocannabinoids produce
anticonvulsant effects through the endocannabinoid system, with few adverse
Conclusion: The endocannabinoid system plays
an active role in seizure termination but does not regulate
Conclusion: Our own results confirm the
overall impression from the literature review of better cognitive performance
in the cannabis user group. A majority of the studies report better cognitive
functioning in the cannabis-related
and psychosis groups compared to non-drug groups.
Conclusion: The first small-scale clinical
studies with CBD treatment of patients with psychotic symptoms further confirm
the potential of CBD as an effective, safe and well-tolerated
Conclusion: Experimental studies show that
cannabidiol reduces psychosis-like effects of
Δ9-tetrahydrocannabinol and synthetic analogs.
Conclusion: our data support the view that
inhibition of microglial activation may improve
Conclusion: Although data available are
sufficient to suggest a possible
involvement of the endogenous cannabinoid system in the neurobiology of
depression, additional studies should be performed in order to better elucidate
the role of this system in the physiopathology of depression.
Conclusion: These findings indicate
antidepressant-like behavioural properties of both THC and rimonabant in OB
rats although additional studies are required to clarify the relationship
between the chronic effects of cannabinoids in other pre-clinical models and in
Conclusion: CBD induces antidepressant-like
effects comparable to those of imipramine. These effects of CBD were probably
mediated by activation of 5-HT(1A) receptors.
Conclusion: Endocannabinoids (ECBs) such as
anandamide (AEA) act by activating cannabinoid type 1 (CB1) or 2 (CB2)
receptors. The anxiolytic effect of drugs that facilitate ECB effects is
associated with increase in AEA levels in several encephalic areas, including
the prefrontal cortex (PFC). We observed that drugs which interfere with ECB
reuptake/metabolism in both the PL and in the dentate gyrus of the dHIP induced
anxiolytic-like effect, in both the EPM and in the VCT via CB1 receptors,
suggesting that CB1 signaling in these brain regions modulates defensive
responses to both innate and learned threatening stimuli. This data further
strengthens previous results indicating modulation of hippocampal and MPFC
activity via CB1 by ECBs, which could be therapeutically targeted to treat
Conclusion: Modulation of hippocampal and
MPFC activity via CB1 by ECBs, which could be therapeutically targeted to treat
The cannabinoid receptor type 1 (CB1)
antagonist SR141716 (3 mg/kg) caused an increase in conditioned freezing upon
repeated tone presentation on three consecutive days. 2-AG fear-promoting
effects depended on CB1 signaling in GABAergic neurons, while an involvement of
glutamatergic neurons remained inconclusive due to the high freezing shown by
amyotrophic lateral sclerosis
Conclusion: Based on the currently available
scientific data, it is reasonable to think that cannabis might significantly
slow the progression of ALS,
potentially extending life expectancy and substantially reducing the overall
burden of the disease.
Conclusion: Although the small number of
people with ALS that reported
using cannabis limits the interpretation of the survey findings, the results
indicate that cannabis may be moderately effective at reducing symptoms of
appetite loss, depression, pain, spasticity, and drooling.
Conclusion: There is evidence that
nabiximols oromucosal spray may reduce subjective symptoms of spasticity and
that dronabinol is effective against neuropathic pain in patients with MS.
Conclusion: Smoked cannabis was superior to
placebo in symptom and
pain reduction in participants with treatment-resistant spasticity.
Conclusion: Cannabinoids inhibit
neurodegeneration in models of
sclerosis. In addition to symptom management, cannabis may also slow the
neurodegenerative processes that ultimately lead to chronic disability in
Conclusion: Our results suggest that JWH-133
acts at CB2 receptors, most likely within the dorsal horn of the spinal cord,
to suppress the hypersensitivity associated with
Conclusion: Parkinson's disease (PD) has a
progressive course and is characterized by the degeneration of
neurons. Although no neuroprotective treatments for PD have been found to
date, the endocannabinoid system has emerged as a promising target. Our
findings point to a possible effect of CBD in improving quality of life
measures in PD patients with no
Conclusion: Significant improvement of sleep
and pain scores. No significant adverse effects of the drug were observed. The
study suggests that cannabis might have a place in the therapeutic
armamentarium of PD.
Conclusion: Given its antioxidant properties
and its ability to activate CB2 but to block CB1 receptors,
Δ9-THCV has a promising pharmacological profile for delaying
disease progression in PD and also for ameliorating parkinsonian symptoms.
Conclusion: Our results support the view of
a potential neuroprotective action of cannabinoids against the in vivo and in
vitro toxicity of 6-hydroxydopamine, which might be relevant for PD. Our data
indicated that these neuroprotective effects might be due, among others, to the
antioxidant properties of certain plant-derived cannabinoids, or exerted
through the capability of cannabinoid agonists to modulate glial function, or
produced by a combination of both mechanisms.
Conclusion: We have demonstrated
up-regulation of the CB1 receptor in direct response to neuronal injury in a
human PD cell culture model, and a direct neuronal protective effect of ??-THC
that may be mediated through PPAR? activation.
Conclusion: These sets of data strongly
suggest that THC could be a potential therapeutic treatment option for
Alzheimer's disease through multiple functions and pathways.
Alzheimer's disease (AD) is characterized by enhanced ß-amyloid peptide
(ßA) deposition along with glial activation in senile plaques, selective
neuronal loss, and cognitive deficits. Cannabinoids are neuroprotective agents
against excitotoxicity in vitro and
damage in vivo. Recent studies on therapeutic strategies for
neurodegenerative diseases such as Parkinson's disease and AD have focused on
the neuroprotective properties (e.g., slowing the ongoing neurodegeneration)
rather than just on palliating symptoms of the diseases (Dawson and Dawson,
2002). Because cannabinoids combine both anti-inflammatory and neuroprotective
actions, our findings may set the basis for the use of these compounds as a
therapeutic approach for AD.
Conclusion: Alzheimer's disease is the
leading cause of
dementia among the elderly, and with the ever-increasing size of this
population, cases of Alzheimer's disease are expected to triple over the next
50 years. AChE inhibitors such as THC and its analogues may provide an improved
therapeutic for Alzheimer's disease, augmenting acetylcholine levels by
degradation and reducing Aß amalgamation, thereby simultaneously treating
both the symptoms and progression of Alzheimer's disease.
Conclusion: Alzheimer's disease (AD) brain
shows an ongoing inflammatory condition and non-steroidal anti-inflammatories
diminish the risk of suffering the neurologic disease. Cannabinoids are
neuroprotective and anti-inflammatory agents with therapeutic potential. We
have shown that chronically administered cannabinoid showed marked beneficial
effects concomitant with inflammation reduction and increased Aß
Conclusion: Currently, the treatment of
Tourette's syndrome (TS) is unsatisfactory. A single-dose, cross-over study in
12 patients, as well as a 6-week, randomised trial in 24 patients, demonstrated
that Δ9-tetrahydrocannabinol (THC), the most psychoactive
ingredient of cannabis, reduces tics in TS patients. No serious adverse effects
occurred and no impairment on neuropsychological performance was